Regulation of energy stores and feeding by neuronal and peripheral CREB activity in Drosophila.

Authors

Koichi Iijima, Laboratory of Neurodegenerative and Metabolic Diseases, Farber Institute for Neurosciences, Department of Biochemistry and Molecular Biology, Thomas Jefferson university, Philadelphia, PAFollow
LiJuan Zhao, Laboratory of Neurodegenerative and Metabolic Diseases, Farber Institute for Neurosciences, Department of Biochemistry and Molecular Biology, Thomas Jefferson university, Philadelphia, PAFollow
Christopher Shenton, Laboratory of Neurogenetics and Pathobiology, Farber Institute for Neurosciences, Department of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PAFollow
Kanae Iijima-Ando, Laboratory of Neurogenetics and Pathobiology, Farber Institute for Neurosciences, Department of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PAFollow

Document Type

Article

Publication Date

12-1-2009

Comments

This article has been peer reviewed and is published in PLoS One 2009, 4(12). The published version is available at DOI: 10.1371/journal.pone.0008498. © Public Library of Science

Abstract

The cAMP-responsive transcription factor CREB functions in adipose tissue and liver to regulate glycogen and lipid metabolism in mammals. While Drosophila has a homolog of mammalian CREB, dCREB2, its role in energy metabolism is not fully understood. Using tissue-specific expression of a dominant-negative form of CREB (DN-CREB), we have examined the effect of blocking CREB activity in neurons and in the fat body, the primary energy storage depot with functions of adipose tissue and the liver in flies, on energy balance, stress resistance and feeding behavior. We found that disruption of CREB function in neurons reduced glycogen and lipid stores and increased sensitivity to starvation. Expression of DN-CREB in the fat body also reduced glycogen levels, while it did not affect starvation sensitivity, presumably due to increased lipid levels in these flies. Interestingly, blocking CREB activity in the fat body increased food intake. These flies did not show a significant change in overall body size, suggesting that disruption of CREB activity in the fat body caused an obese-like phenotype. Using a transgenic CRE-luciferase reporter, we further demonstrated that disruption of the adipokinetic hormone receptor, which is functionally related to mammalian glucagon and beta-adrenergic signaling, in the fat body reduced CRE-mediated transcription in flies. This study demonstrates that CREB activity in either neuronal or peripheral tissues regulates energy balance in Drosophila, and that the key signaling pathway regulating CREB activity in peripheral tissue is evolutionarily conserved.

Recommended Citation

Iijima, Koichi; Zhao, LiJuan; Shenton, Christopher; and Iijima-Ando, Kanae, "Regulation of energy stores and feeding by neuronal and peripheral CREB activity in Drosophila." (2009). Department of Biochemistry and Molecular Biology Faculty Papers. Paper 29.
https://jdc.jefferson.edu/bmpfp/29

PubMed ID

20041126